Ankylosing Spondylitis and Gout

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  • Created by: LBCW0502
  • Created on: 07-02-19 17:10
What is ankylosing spondylitis? (1)
Type of arthritis that mainly affects the back. Inflammation of the spine. Bone growing from sides of vertebrae which fuse together. Starts in joints between spine and pelvis (sacroiliac). Auto-immune inflammatory reaction
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What is ankylosing spondylitis? (2)
Ca deposits in area, bone fuses together, restricts bending/movement of spine (main symptoms - pain and stiffness)
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Describe the epidemiology of AS
0.05-0.23% of population, disease mainly affects young people. Onset average of 24 years. Men 3x more likely to get AS compared to women
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What are the symptoms of AS? (1)
Sacroilitis (inflammation of sacroiliac joints - causes lower back/buttocks pain extending to legs). Inflammation rises up spine, pain/stiffness/fatigue/inflammation at entheses (connective tissue). Other joints can be involved
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What are the symptoms of AS? (2)
Heel tenderness, swollen fingers and toes, chest tightness, eye inflammation (uveitis)
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Describe features of diagnosing AS
Based on symptoms (age, inflammatory stiffness, morning onset, FH). X-ray/MRI of spine/sacroiliac joints. Inflammation (CRP, ESR), HLAB27 (associated with leukocyte antigen)
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How is the disease assessed?
Modified NY criteria. ASAS classification criteria for axial spondyloarthritis, BASDAI (fatigue, spinal, joint pain, tenderness, duration, severity, score out of 10) and VAS (six questions, score out of 10, patient chooses score)
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Describe the differential diagnosis for AS
Mechanical back pain, psoriatic arthritis, reactive arthritis, inflammatory bowel disease, RA, infections, cancer
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What are the treatment options for AS? (1)
First line - NSAIDs (e.g. modified release, paracetamol/codeine, PPI). Local corticosteroids, DMARDs/biologics (if uncontrolled), physiotherapy, bisphosphonates
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What are the treatment options for AS? (2)
NICE guidelines – look at extent of how scores decrease (by 50%) to continue therapy
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What is the second line treatment for AS?
Anti-TNF drugs (if patient fails to respond to NSAIDs). Adalimumab, entanercept, golimumab, infliximab, certolizumab. Secukinumab (IL-7 inhibitor). Re-assess at 12 weeks (16 weeks for Secukinumab)
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What is gout?
Form of inflammatory arthritis, disorder of purine metabolism (raised uric acid levels). Deposition of urate crystals in synovial fluid and other tissues.
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Describe the prevalence of AS
Most common inflammatory arthritis, affects 2% of adults in developed countries (due to diet). Increases with age. More common in men than women. Increased due to ageing population, increased obesity/dietary changes. Recurrent attacks are common
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What are the risks factors for gout? (1)
Drugs - thiazide diuretics (Bendroflumethiazide – can increase likelihood of patient experiencing gout, CI), low dose aspirin, ciclosporin. Co-morbidities (diabetes, obesity, hyperlipidaemia, renal impairment, hypertension, heart failure)
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What are the risks factors for gout? (2)
Diet (meat, seafood, beer, spirits, coffee, dairy products, vitamin C reduce urate levels). Genetics polymorphisms (involved in renal urate transport)
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What are the signs and symptoms of gout? (1)
Intense rapidly developing severe pain in joint (often starts in big toe). Hot/extremely tender. Swollen. Skin appears red/shiny, usually starts at night, hyperuricaemia, joint X-rays, synovial fluid
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What are the signs and symptoms of gout? (2)
Septic arthritis – take cultures (find infection, crystals) – when treatment for gout is not effective
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Serum urate levels of >7 mg/dL indicates what?
Hyperuricaemia (due to under excretion or over production). Urate is a product of purine metabolism, adenine/guanine (nucleotide bases), intake from diet
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What is the target for serum urate levels in patients with gout?
<6 mg/dL. (Patients may have high levels of uric acid but doesn’t have gout/link to chronic kidney disease possibly)
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Outline the uric acid production pathway
Purine nucleoside metabolism - xanthine - (xanthine oxidase) - uric acid - 1. renal excretion/uricosuria, 2. GI excretion, 3. circulating in excess/urate deposition/tophi/inflammatory activation with acute gout attack
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Describe features of phase 1 gout
Intermittent acute attacks, resolving spontaneously over 7-10 days, asymptomatic between attacks
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Describe features of phase 2 gout
Chronic tophaceous gout, often polyarticular attacks. Symptomatic in between (acute attacks). Crystal deposition (tophi) in soft tissues or joints - caused by no treatment/ineffective treatment of gout
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What are the goals of therapy for gout?
Modification of risk factors. Symptom relief for acute gout flares. Long-term treatment for chronic hyperuricaemia
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What are the lifestyle modifications which can be made to diet (non-pharmacological treatments for gout)?
Reduce red meat and alcohol, be at ideal body weight, stay hydrated (dehydration increases levels of uric acid), carbohydrates and vitamin C in diet
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What self-care advice can be offered to patients who have gout? (1)
Advise to rest and elevate the limb. Avoid trauma to affected joint. Keep joint in a cool environment by not covering (e.g. sock, show, bed clothing) and use ice pack for 20 mins repeated as often as required
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What self-care advice can be offered to patients who have gout? (2)
Discuss lifestyle issues (weight loss, exercise, diet, alcohol consumption, fluid intake)
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How is acute gout managed?
NSAIDs (first line - maximum dose used). Colchine. Glucocorticoids (oral, intra-articular). Measure uric acid levels 4-6 weeks after acute attack
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Describe features of NSAIDs used to manage acute gout (1)
Naproxen (500 mg BD for 5 days). Ibuprofen (1200 mg OD). Indometacin (50 mg TDS, 2 days, then 25 mg TDS for 3 days). Avoid in renal/hepatic impairment, bleeding disorders, CCF, allergy, increased thrombotic events, GI bleeding, co-administer with PPI
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Describe features of NSAIDs used to manage acute gout (2)
Continue all NSAIDs for 48 hours after attack is resolved. Don’t have to add on a PPI (depending on age) due to being a short course
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Describe features of colchicine (1)
Second line/due to toxicity at higher doses (used - NSAID CI or ineffective). Inhibits neutrophil motility/activity leading to anti-inflammatory effect. 500 mcg oral 2-4 x day until symptoms resolved. Max 6 mg per course, not repeated within 3 days
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Describe features of colchicine (2)
But can be used for long term/requires specialist. Main adverse effect is GI. E.g. diarrhoea, nausea, vomiting (counselling)
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Describe features of corticosteroids
Used when NSAIDs/colchicine poorly tolerated/CI. Poor evidence for IA/IM. PO prednisolone 30 mg OD for 5 days. Caution - hyperglycaemia, CCF, may use in moderate-severe renal impairment. Monitor 4-6 weeks later (check serum level target)
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Describe features for management of chronic hyperuricaemia
Aim to prevent acute flares/tophi and serum urate of < 6 mg/dL. Start urate-lowering therapy (ULT) if 2+ attacks/year or presence of tophi. Need to consider frequency, risk factors, severity of attacks
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Describe features of ULT (1)
Start 2-4 weeks after flare resolved. Continue flare NSAIDs/colchicine therapy. Xanthine oxidase inhibitors (block synthesis of uric acid). Allopurinol (first line), febuoxstat (second line). Uricosuric agents (increase excretion in urine
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Describe features of ULT (2)
Benzbromarone, sulfinpyrazone. Life long treatment - consider reducing dose to maintain low serum uric acid level
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Describe features of allopurinol (1)
Purine analogue. Pro-drug (oxypurinol active moiety). Effective at decreasing flares/tophi. 2% get rash. Severe hypersensitivity rare (can be life threatening). Dose reduction in renal impairment. Only start when acute attack resolves
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Describe features of allopurinol (2)
Check allergy status, renal clearance (check patients with CKD).
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Describe features of febuxostat (1)
(2nd line/more likely to have flares). Non-purine potent inhibitor of xanthine oxidase. 2.3 - 3 x more likely to achieve target serum urate levels at 1 year than allopurinol. Start 1-2 weeks after inflammation settled, increase dose after 2-4 weeks
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Describe features of febuxostat (2)
Dose adjustment needed in mild-moderate renal impairment. Liver function test (monitoring)
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What is the role of uricosurics?
Promotes excretion of uric acid, works at transporters in kidneys, prevents reabsorption of uric acid. E.g. probenecid, benzbromarone
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Describe features of benzbromarone (1)
Potent uricosuric (block renal tubular urate reabsorption). Withdrawn in 2003 in some countries due to hepatoxicity. Close monitoring of liver function/slow dose escalation. Used as unlicensed medicine on named patient basis. 100-200 mg OD
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Describe features of benzbromarone (2)
Useful for patients with renal impairment
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Outline the mechanism for uric acid production and elimination (1)
Adenosine - inosine - hypoxanthine - uric acid - excretion via URAT1 or urate oxidase. Allopurinol/febuxostat target xanthine oxidase. Probenecid/benzbromarone target URAT1. Pegloticase targets urate oxidase
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Outline the mechanism for uric acid production and elimination (2)
Combining dual mechanisms of xanthine oxidase and URAT1 inhibitor can produce greater reductions of uric acid than can be achieved with standard doses of either agent alone
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Which medicine is not NICE recommended/authorised?
Pegloticase
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What are the other treatment options for gout? (1)
Lesinurad (urate transporter-1 inhibitor blocks reabsorption of urate, addition to xanthine oxidase inhibitors, no longer recommended within its MA with a xanthine oxidase inhibitor for treating hyperuricaemia in adults with gout).
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What are the other treatment options for gout? (2)
Lesinurad – used with allopurinol, serum uric level is reduced more but clinical symptoms do not improve (when using allopurinol alone)
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What are the other treatment options for gout? (3)
Losartan (Ca channel blockers increase uric acid excretion). Fenofibrate (with urate lowering agents) - reduce urate through uricosuric actions but not known if they reduce frequency
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What are the other treatment options for gout? (4)
Fenofibrate is useful in treatment of resistant cases or where hypertension/hyperlipidaemia are co-morbidities
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Describe features of flare prophylaxis during initiation of ULT (1)
Rapidly lowering urate levels is associated with gout flares - need prophylactic cover (NSAID/colchicine). Colchicine 500 mg BD for 6 months or low dose NSAIDs for 6+ weeks when starting allopurinol/febuxostat
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Describe features of flare prophylaxis during initiation of ULT (2)
May need longer if tophi present until tophus is resolved. Where a flare occurs in a patient stabilised on either allopurinol or febuxostat - do not stop these agents
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Card 2

Front

What is ankylosing spondylitis? (2)

Back

Ca deposits in area, bone fuses together, restricts bending/movement of spine (main symptoms - pain and stiffness)

Card 3

Front

Describe the epidemiology of AS

Back

Preview of the front of card 3

Card 4

Front

What are the symptoms of AS? (1)

Back

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Card 5

Front

What are the symptoms of AS? (2)

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